Component

Cell proliferation

Increase in cultured-cell number through cell division.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Increasing extracellular Mg restored proliferation and viability of TRPM7-deficient DT40 cells.

    Mg2+ → Cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Extracellular magnesium supplementation after TRPM7 disruption
    experimental_model
    Extracellular magnesium supplementation after TRPM7 disruption
    limitations
    Culture rescue is not a clinical dose recommendation or evidence all TRPM7 functions are Mg-dependent.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Chicken
    plain_language
    Additional magnesium bypassed enough of the transport defect to restore cultured-cell growth.
    primary_references
    [schmitz-2003-trpm7] Regulation of vertebrate cellular Mg2+ homeostasis by TRPM7 (2003). https://pubmed.ncbi.nlm.nih.gov/12887921/ DOI: 10.1016/S0092-8674(03)00556-7
    tissue
    DT40 B-cell culture
    tissue_or_cell_type
    DT40 B-cell culture
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 962–973

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Extracellular magnesium supplementation after TRPM7 disruption · source_derived_draft · unverified_draft

    ### magnesium-rescues-trpm7-cell-proliferation Increasing extracellular Mg restored proliferation and viability of TRPM7-deficient DT40 cells. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Additional magnesium bypassed enough of the transport defect to restore cultured-cell growth. organism: Chicken tissue_or_cell_type: DT40 B-cell culture experimental_model: Extracellular magnesium supplementation after TRPM7 disruption limitations: Culture rescue is not a clinical dose recommendation or evidence all TRPM7 functions are Mg-dependent. evidence-system: Extracellular magnesium supplementation after TRPM7 disruption tissue: DT40 B-cell culture [schmitz-2003-trpm7] Regulation of vertebrate cellular Mg2+ homeostasis by TRPM7 (2003). https://pubmed.ncbi.nlm.nih.gov/12887921/ DOI: 10.1016/S0092-8674(03)00556-7
    Complete structured claim and evidence

  2. DIM at 10 micromolar increased proliferation in estrogen-deprived breast-cancer cells; an ERalpha antagonist blocked the response.

    3,3'-Diindolylmethane / DIM → Cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/25048790.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17", "start_char": 0, "end_char": 1824, "text_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17"}
    experimental_model
    Gene expression, chromatin, inhibitors and growth assays
    exposure
    DIM 10 versus 50 micromolar; estradiol absent
    limitations
    The authors call 10 micromolar obtainable, but this is not a demonstrated human tissue concentration or clinical tumor outcome. Estrogen context and concentration matter.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human MCF-7 and T47D cells
    plain_language
    A growth-promoting response appeared under one defined hormonal condition.
    primary_references
    [dim-p25048790] Low levels of 3,3'-diindolylmethane activate estrogen receptor α and induce proliferation of breast cancer cells in the absence of estradiol. (2014). https://pubmed.ncbi.nlm.nih.gov/25048790/ DOI: 10.1186/1471-2407-14-524
    tissue_or_cell_type
    ERalpha and proliferation

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 610–621

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene expression, chromatin, inhibitors and growth assays · source_derived_draft · unverified_draft

    ### dim-eralpha-proliferation DIM at 10 micromolar increased proliferation in estrogen-deprived breast-cancer cells; an ERalpha antagonist blocked the response. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A growth-promoting response appeared under one defined hormonal condition. organism: Human MCF-7 and T47D cells tissue_or_cell_type: ERalpha and proliferation experimental_model: Gene expression, chromatin, inhibitors and growth assays limitations: The authors call 10 micromolar obtainable, but this is not a demonstrated human tissue concentration or clinical tumor outcome. Estrogen context and concentration matter. exposure: DIM 10 versus 50 micromolar; estradiol absent evidence_span: {"source_cache": "artifacts/dim-research/25048790.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17", "start_char": 0, "end_char": 1824, "text_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17"} [dim-p25048790] Low levels of 3,3'-diindolylmethane activate estrogen receptor α and induce proliferation of breast cancer cells in the absence of estradiol. (2014). https://pubmed.ncbi.nlm.nih.gov/25048790/ DOI: 10.1186/1471-2407-14-524
    Complete structured claim and evidence

  3. DIM inhibited estradiol-induced MCF-7 proliferation in the tested estrogen-stimulated system.

    3,3'-Diindolylmethane / DIM → Cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/9771935.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799", "start_char": 0, "end_char": 1556, "text_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799"}
    experimental_model
    Ligand binding, nuclear complex, transcription and growth assays
    exposure
    DIM 10-50 micromolar in cells; rodent dosing separately
    limitations
    Preclinical evidence. Estrogen exposure, tissue and concentrations affect the response; no human cancer-treatment efficacy established.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human MCF-7 cells and rat mammary-tumor model
    plain_language
    Its effect depended on the hormonal conditions being tested.
    primary_references
    [dim-p9771935] Aryl hydrocarbon receptor-mediated antiestrogenic and antitumorigenic activity of diindolylmethane. (1998). https://pubmed.ncbi.nlm.nih.gov/9771935/ DOI: 10.1093/carcin/19.9.1631
    tissue_or_cell_type
    AhR and estrogen-responsive signaling

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 311–322

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ligand binding, nuclear complex, transcription and growth assays · source_derived_draft · unverified_draft

    ### dim-estrogen-growth-inhibition DIM inhibited estradiol-induced MCF-7 proliferation in the tested estrogen-stimulated system. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Its effect depended on the hormonal conditions being tested. organism: Human MCF-7 cells and rat mammary-tumor model tissue_or_cell_type: AhR and estrogen-responsive signaling experimental_model: Ligand binding, nuclear complex, transcription and growth assays limitations: Preclinical evidence. Estrogen exposure, tissue and concentrations affect the response; no human cancer-treatment efficacy established. exposure: DIM 10-50 micromolar in cells; rodent dosing separately evidence_span: {"source_cache": "artifacts/dim-research/9771935.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799", "start_char": 0, "end_char": 1556, "text_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799"} [dim-p9771935] Aryl hydrocarbon receptor-mediated antiestrogenic and antitumorigenic activity of diindolylmethane. (1998). https://pubmed.ncbi.nlm.nih.gov/9771935/ DOI: 10.1093/carcin/19.9.1631
    Complete structured claim and evidence

  4. DIM at 50 micromolar inhibited proliferation in contrast with the lower-concentration response.

    3,3'-Diindolylmethane / DIM → Cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/25048790.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17", "start_char": 0, "end_char": 1824, "text_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17"}
    experimental_model
    Gene expression, chromatin, inhibitors and growth assays
    exposure
    DIM 10 versus 50 micromolar; estradiol absent
    limitations
    The authors call 10 micromolar obtainable, but this is not a demonstrated human tissue concentration or clinical tumor outcome. Estrogen context and concentration matter.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human MCF-7 and T47D cells
    plain_language
    Direction changed with concentration within the same experimental study.
    primary_references
    [dim-p25048790] Low levels of 3,3'-diindolylmethane activate estrogen receptor α and induce proliferation of breast cancer cells in the absence of estradiol. (2014). https://pubmed.ncbi.nlm.nih.gov/25048790/ DOI: 10.1186/1471-2407-14-524
    tissue_or_cell_type
    ERalpha and proliferation

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 636–647

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene expression, chromatin, inhibitors and growth assays · source_derived_draft · unverified_draft

    ### dim-higher-dose-growth-inhibition DIM at 50 micromolar inhibited proliferation in contrast with the lower-concentration response. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Direction changed with concentration within the same experimental study. organism: Human MCF-7 and T47D cells tissue_or_cell_type: ERalpha and proliferation experimental_model: Gene expression, chromatin, inhibitors and growth assays limitations: The authors call 10 micromolar obtainable, but this is not a demonstrated human tissue concentration or clinical tumor outcome. Estrogen context and concentration matter. exposure: DIM 10 versus 50 micromolar; estradiol absent evidence_span: {"source_cache": "artifacts/dim-research/25048790.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17", "start_char": 0, "end_char": 1824, "text_sha256": "3729748e0cd55782230ad119eddfb3a79e0cdfd78503f5dbf397ae0ab5f68a17"} [dim-p25048790] Low levels of 3,3'-diindolylmethane activate estrogen receptor α and induce proliferation of breast cancer cells in the absence of estradiol. (2014). https://pubmed.ncbi.nlm.nih.gov/25048790/ DOI: 10.1186/1471-2407-14-524
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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